The super-cell plane wave expansion method is employed to calculate band structures for the design of a siliconbased one-dimensional phononic crystal plate with large absolute forbidden bands. In this method, a low im...The super-cell plane wave expansion method is employed to calculate band structures for the design of a siliconbased one-dimensional phononic crystal plate with large absolute forbidden bands. In this method, a low impedance medium is introduced to replace the free stress boundary, which largely reduces the computational complexity. The dependence of band gaps on structural parameters is investigated in detail. To prove the validity of the super-cell plane wave expansion, the transmitted power spectra of the Lamb wave are calculated by using a finite element method. With the detailed computation, the band-gap of a one-dimensional plate can be designed as required with appropriate structural parameters, which provides a guide to the fabrication of a Lamb wave phononic crystal.展开更多
The pathology of Alzheimer’s disease involves a long preclinical period,where the characteristic clinical symptoms of the changes in the brain are undetectable.During the preclinical period,homeostatic mechanisms may...The pathology of Alzheimer’s disease involves a long preclinical period,where the characteristic clinical symptoms of the changes in the brain are undetectable.During the preclinical period,homeostatic mechanisms may help prevent widespread cell death.Evidence has pointed towards selective cell death of diseased neurons playing a potentially protective role.As the disease progresses,dysregulation of signaling pathways that govern cell death contributes to neurodegeneration.Aberrant activation of the c-Jun N-terminal kinase pathway has been established in human and animal models of Alzheimer’s disease caused by amyloid-beta 42-or tau-mediated neurodegeneration.Clonal mosaic studies in Drosophila that examine amyloid-beta 42 in a subset of neurons suggest complex interplay between amyloid-beta 42-expressing and wild-type cells.This review examines the role of c-Jun N-terminal kinase signaling in the context of cell competition and short-range signaling interactions between amyloid-beta 42-expressing and wild-type neurons.Cell competition is a conserved phenomenon regulating tissue integrity by assessing the fitness of cells relative to their neighbors and eliminating suboptimal cells.Somatic clones of amyloid-beta 42 that juxtapose genetically distinct neuronal cell populations show promise for studying neurodegeneration.Generating genetic mosaics with labeled clones of amyloid-beta 42-or tau-expressing and wild-type neurons will allow us to understand how short-range signaling alterations trigger cell death in neurons and thereby contribute to the progression of Alzheimer’s disease.These approaches have the potential to uncover biomarkers for early Alzheimer’s disease detection and new therapeutic targets for intervention.展开更多
AIM:To evaluate tracking of magnetically labeled mesenchymal stem cells(MSCs) after intraportal transplantation.METHODS:Mononuclear cells were isolated from bone marrow aspirates of pigs by density gradient centrifuga...AIM:To evaluate tracking of magnetically labeled mesenchymal stem cells(MSCs) after intraportal transplantation.METHODS:Mononuclear cells were isolated from bone marrow aspirates of pigs by density gradient centrifugation,cultured and expanded,after which,they were incubated with super paramagnetic iron oxide(SPIO).Prussian blue staining was performed to highlight intracellular iron.To establish swine models of acute liver injury,0.5 g/kg D-galactosamine was administrated to 10 pigs,six of which were injected via their portal veins with SPIO-labeled MSCs,while the remaining four were injected with unlabeled cells.Magnetic resonance imaging(MRI) was performed with a clinical 1.5T MR scanner immediately before transplantation and 6 h,3 d,7 d and 14 d after transplantation.Prussian blue staining was again performed with the tissue slices at the endpoint.RESULTS:Prussian blue staining of SPIO-labeled MSCs had a labeling efficiency of almost 100%.Signal intensity loss in the liver by SPIO labeling on the FFE(T2*WI) sequence persisted until 14 d after transplantation.Histological analysis by Prussian blue staining confirmed homing of labeled MSCs in the liver after 14 d;primarily distributed in hepatic sinusoids and liver parenchyma.CONCLUSION:MSCs were successfully labeled with SPIO in vitro.MRI can monitor magnetically labeled MSCs transplanted into the liver.展开更多
The separation, extraction of lycopene and its effects on the proliferation and cells cycle of the chemical-induced cells were investigated in order to research on its extraction method and the mechanism in inhibiting...The separation, extraction of lycopene and its effects on the proliferation and cells cycle of the chemical-induced cells were investigated in order to research on its extraction method and the mechanism in inhibiting neoplastic transformation. The best extraction condition of lycopene with super-critical carbon dioxide was under the pressure of 25MPa, the temperature of 50℃ and duration of 3. 0h. Lycopene could inhibit cell growth rate and cells proliferation significantly, while increase the cell numbers of G1 -phase and decrease that of S-phase and G2+M-phase. The potency of the effects of lycopene on cells cycle might be one of the important reasons for inhibiting neoplastic transformation.展开更多
Objective:To investigate the effect of SHU555A,a clinically approved iron nanoparticle,labeling on differentiation of bone marrow mesenchymal stem cells(BMSCs) into neurocyte-like cells in vitro.Methods:10 times dilut...Objective:To investigate the effect of SHU555A,a clinically approved iron nanoparticle,labeling on differentiation of bone marrow mesenchymal stem cells(BMSCs) into neurocyte-like cells in vitro.Methods:10 times dilution of 10μl,20μl,40μl and 80μl SHU555A were added to 2ml of culture medium containing rat BMSCs to obtain four experimental groups of SHU555A labeling of BMSCs with ferri ion concentrations of 14μg/ml,28μg/ml,56μg/ml and 112μg/ml,respectively.2ml of culture medium with rat BMSCs did not contain SHU555A served as control group.The BMSCs of all the groups were pre-induced by bFGF,and induced by DMSO/butylated hydroxyanisole(BHA) for six hours,subsequently reverse transcription polymerase chain reaction(RT-PCR) technique was employed to detect mRNA expression of nestin,neuronspecific analase(NSE) and glial fibrillary acid protein(GFAP).Western blot technique was used to detectprotein expression of nestin.Results:Quantitative-PCR revealed high mRNA expression of nestin,NSE and GFAP induced by DMSO/BHA in all the experimental groups,but the difference between the experimental groups and the control group was not significant(P>0.05).Western blot analysis demonstrated there was no statistically significant difference in nestin protein expression between the experimental groups and the control group(P>0.05).Conclusion:SHU555A labeling do not affect differentiation of rat BMSCs into neurocyte-like cells in vitro.展开更多
基金Project supported by the National Natural Science Foundation of China (Grant Nos. 10874086 and 10834009)the National Basic Research Program of China (Grant No. 2010CB327803)
文摘The super-cell plane wave expansion method is employed to calculate band structures for the design of a siliconbased one-dimensional phononic crystal plate with large absolute forbidden bands. In this method, a low impedance medium is introduced to replace the free stress boundary, which largely reduces the computational complexity. The dependence of band gaps on structural parameters is investigated in detail. To prove the validity of the super-cell plane wave expansion, the transmitted power spectra of the Lamb wave are calculated by using a finite element method. With the detailed computation, the band-gap of a one-dimensional plate can be designed as required with appropriate structural parameters, which provides a guide to the fabrication of a Lamb wave phononic crystal.
基金supported by 1RO1EY032959-01,NIH1R15GM124654-01 from NIHSchuellein Chair Endowment Fund and STEM Catalyst Grant and start-up support from the University of Dayton(to AS,MKS is Co-PI on NIH RO1 and Co-I on NIH R15)。
文摘The pathology of Alzheimer’s disease involves a long preclinical period,where the characteristic clinical symptoms of the changes in the brain are undetectable.During the preclinical period,homeostatic mechanisms may help prevent widespread cell death.Evidence has pointed towards selective cell death of diseased neurons playing a potentially protective role.As the disease progresses,dysregulation of signaling pathways that govern cell death contributes to neurodegeneration.Aberrant activation of the c-Jun N-terminal kinase pathway has been established in human and animal models of Alzheimer’s disease caused by amyloid-beta 42-or tau-mediated neurodegeneration.Clonal mosaic studies in Drosophila that examine amyloid-beta 42 in a subset of neurons suggest complex interplay between amyloid-beta 42-expressing and wild-type cells.This review examines the role of c-Jun N-terminal kinase signaling in the context of cell competition and short-range signaling interactions between amyloid-beta 42-expressing and wild-type neurons.Cell competition is a conserved phenomenon regulating tissue integrity by assessing the fitness of cells relative to their neighbors and eliminating suboptimal cells.Somatic clones of amyloid-beta 42 that juxtapose genetically distinct neuronal cell populations show promise for studying neurodegeneration.Generating genetic mosaics with labeled clones of amyloid-beta 42-or tau-expressing and wild-type neurons will allow us to understand how short-range signaling alterations trigger cell death in neurons and thereby contribute to the progression of Alzheimer’s disease.These approaches have the potential to uncover biomarkers for early Alzheimer’s disease detection and new therapeutic targets for intervention.
基金Supported by (partly) the Natural Science Foundation of Jiangsu Province, No BK2007537key program of Nanjing Municipal Bureau of Public Health, No ZKX06015
文摘AIM:To evaluate tracking of magnetically labeled mesenchymal stem cells(MSCs) after intraportal transplantation.METHODS:Mononuclear cells were isolated from bone marrow aspirates of pigs by density gradient centrifugation,cultured and expanded,after which,they were incubated with super paramagnetic iron oxide(SPIO).Prussian blue staining was performed to highlight intracellular iron.To establish swine models of acute liver injury,0.5 g/kg D-galactosamine was administrated to 10 pigs,six of which were injected via their portal veins with SPIO-labeled MSCs,while the remaining four were injected with unlabeled cells.Magnetic resonance imaging(MRI) was performed with a clinical 1.5T MR scanner immediately before transplantation and 6 h,3 d,7 d and 14 d after transplantation.Prussian blue staining was again performed with the tissue slices at the endpoint.RESULTS:Prussian blue staining of SPIO-labeled MSCs had a labeling efficiency of almost 100%.Signal intensity loss in the liver by SPIO labeling on the FFE(T2*WI) sequence persisted until 14 d after transplantation.Histological analysis by Prussian blue staining confirmed homing of labeled MSCs in the liver after 14 d;primarily distributed in hepatic sinusoids and liver parenchyma.CONCLUSION:MSCs were successfully labeled with SPIO in vitro.MRI can monitor magnetically labeled MSCs transplanted into the liver.
基金supported by China Postdoctoral Science Foundation
文摘The separation, extraction of lycopene and its effects on the proliferation and cells cycle of the chemical-induced cells were investigated in order to research on its extraction method and the mechanism in inhibiting neoplastic transformation. The best extraction condition of lycopene with super-critical carbon dioxide was under the pressure of 25MPa, the temperature of 50℃ and duration of 3. 0h. Lycopene could inhibit cell growth rate and cells proliferation significantly, while increase the cell numbers of G1 -phase and decrease that of S-phase and G2+M-phase. The potency of the effects of lycopene on cells cycle might be one of the important reasons for inhibiting neoplastic transformation.
基金Henan ontstanding talent program(084200510012)zhou research programs(083SGYS33262-5)zhou university 2011 project,third constraction projection:basic and clinical research of stem cell
文摘Objective:To investigate the effect of SHU555A,a clinically approved iron nanoparticle,labeling on differentiation of bone marrow mesenchymal stem cells(BMSCs) into neurocyte-like cells in vitro.Methods:10 times dilution of 10μl,20μl,40μl and 80μl SHU555A were added to 2ml of culture medium containing rat BMSCs to obtain four experimental groups of SHU555A labeling of BMSCs with ferri ion concentrations of 14μg/ml,28μg/ml,56μg/ml and 112μg/ml,respectively.2ml of culture medium with rat BMSCs did not contain SHU555A served as control group.The BMSCs of all the groups were pre-induced by bFGF,and induced by DMSO/butylated hydroxyanisole(BHA) for six hours,subsequently reverse transcription polymerase chain reaction(RT-PCR) technique was employed to detect mRNA expression of nestin,neuronspecific analase(NSE) and glial fibrillary acid protein(GFAP).Western blot technique was used to detectprotein expression of nestin.Results:Quantitative-PCR revealed high mRNA expression of nestin,NSE and GFAP induced by DMSO/BHA in all the experimental groups,but the difference between the experimental groups and the control group was not significant(P>0.05).Western blot analysis demonstrated there was no statistically significant difference in nestin protein expression between the experimental groups and the control group(P>0.05).Conclusion:SHU555A labeling do not affect differentiation of rat BMSCs into neurocyte-like cells in vitro.
